LncRNA MEG3 inhibits non-small cell lung cancer via interaction with DKC1 protein.

Abstract

Long non-coding RNA (lncRNA) MEG3 is a key biomarker and therapeutic target in lung cancer; however, its underlying molecular mechanism in lung cancer progression remains unclear. The present study demonstrated a novel regulatory axis in lung cancer, lncRNA MEG3/dyskeratosis congenita 1 (DKC1), and further investigated the effects and molecular mechanism of lncRNA MEG3/DKC1 in lung cancer. RT-qPCR and western blot analysis were performed to determine gene and protein expression levels. The RNA immunoprecipitation assay was performed to verify binding between lncRNA MEG3 and DKC1. Flow cytometry analysis was performed to assess cell apoptosis, while the Cell Counting Kit-8 assay was performed to determine cell viability. Transwell and wound healing assays were performed to assess cell invasion and migration, respectively. Telomerase activity was measured using the quantitative TeloTAGGG Telomerase PCR-ELISA kit. The results demonstrated that lncRNA MEG3 was downregulated, while its binding protein, DKC1, was upregulated in lung cancer cells. Furthermore, lncRNA MEG3 inhibited cell proliferation, migration, invasion and telomerase activity in A549 cells by downregulating DKC1. lncRNA MEG3 inhibited non-small cell lung cancer progression by inhibiting telomere function, cell proliferation, telomerase activity, cell migration and invasion via regulation of the DKC1 protein expression. LncRNA MEG3/DKC1 was identified as a novel dual-directional regulatory axis in the present study, acting as a promising target for the treatment of lung cancer.